Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2003 Mar;108(3):263-73.
doi: 10.1046/j.1365-2567.2003.01592.x.

B cell inhibitory receptors and autoimmunity

Nicholas R Pritchard  1 , Kenneth G C Smith
Affiliations
Review

B cell inhibitory receptors and autoimmunity

Nicholas R Pritchard et al. Immunology. 2003 Mar.
No abstract available

PubMed Disclaimer

Figures

Figure 1
Figure 1
B cell inhibitory receptors.
Figure 2
Figure 2
The FcγRII inhibitory pathway. Cross-linking of FcγRII to the BCR by immune complexes containing IgG inhibits B cell activation. This occurs through a number of mechanisms that are mediated by SHIP and lyn at key stages.
Figure 3
Figure 3
The CD22 inhibitory pathway. Ligation of CD22 to the BCR and subsequent SHP-1 activation by lyn inhibits B cell activation through a number of mechanisms.
Figure 4
Figure 4
SLE in mice and humans. (a) Antinuclear antibodies in the serum of Lyn deficient mice, shown binding to HEp2 cells (courtesy of Dr D. M. Tarlinton). (b) Immunofluorescence microscopy for IgG demonstrating the deposition of immune complexes in a glomerulus from an SLE patient with membranous (Type V) lupus nephritis. (c) A normal glomerulus. (d) A glomerulus from a patient with SLE showing the inflammatory response to immune complex deposition (diffuse proliferative glomerulonephritis). (e) Crescentic glomerulonephritis with scarring following lupus glomerulonephritis. (f) Discoid lupus; a form of skin rash seen in SLE.
Figure 5
Figure 5
The pathogenesis of SLE. The breakdown in tolerance responsible for the development of autoantibodies (upper panel) is necessary but insufficient to cause disease in the absence of an abnormal inflammatory response to immune complexes (lower panel). Cell types in which FcγRIIb is likely to control antibody production or immune complex handling are shown in red.
See this image and copyright information in PMC

References

    1. Muta T, Kurosaki T, Misulovin Z, Sanchez M, Nussenzweig MC, Ravetch JV. A 13-amino-acid motif in the cytoplasmic domain of Fc gamma RIIB modulates B-cell receptor signalling. Nature. 1994;368:70–3. - PubMed
    1. Doody GM, Justement LB, Delibrias CC, Matthews RJ, Lin J, Thomas ML, Fearon DT. A role in B cell activation for CD22 and the protein tyrosine phosphatase SHP. Science. 1995;269:242–4. - PubMed
    1. Smith KGC, Tarlinton DM, Doody GM, Hibbs ML, Fearon DT. Inhibition of the B cell by CD22: a requirement for Lyn. J Exp Med. 1998;187:807–11. - PMC - PubMed
    1. Tamir I, Dal Porto JM, Cambier JC. Cytoplasmic protein tyrosine phosphatases SHP-1 and SHP-2: regulators of B cell signal transduction. Curr Opin Immunol. 2000;12:307–15. - PubMed
    1. Daeron M. Fc receptor biology. Annu Rev Immunol. 1997;15:203–34. - PubMed

LinkOut - more resources